Chronic Kidney Disease Models and Therapeutic Interventions
Summary
Chronic kidney disease encompasses a spectrum of disorders leading to gradual loss of renal function, driven by intricate mechanisms including inflammation, oxidative stress and fibrogenesis. Animal and in vitro models are indispensable for dissecting these pathways and for preclinical evaluation of therapeutics. Traditional paradigms include 5/6 nephrectomy and adenine-enriched diets that recapitulate tubulointerstitial fibrosis, tubular atrophy and glomerulosclerosis. Recent refinements exploit alternative mouse strains and recovery protocols to better mirror human CKD variability and assess regenerative potential. Therapeutic interventions have expanded beyond renin–angiotensin system blockade to encompass sodium–glucose cotransporter 2 inhibitors, anti-fibrotic small molecules, sirtuin modulators and monoclonal antibodies targeting profibrotic cytokines. Emerging strategies focus on restoring mitochondrial integrity, modulating aquaporin trafficking to recover water homeostasis and curbing leukocyte infiltration via cell adhesion molecule interference. Together, these models and interventions form a robust framework for translating basic insights into clinical innovations to delay CKD progression and mitigate global disease burden.
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Chronic Kidney Disease Models and Therapeutic Interventions publication trend
The graph below shows the total number of articles in chronic kidney disease models and therapeutic interventions across all publications each year (not limited to Nature Index journals).
Technical terms
Adenine-induced model: Dietary supplementation with adenine to induce renal injury characterised by tubular damage, fibrosis and inflammation in rodents.
Tubulointerstitial fibrosis: Excessive deposition of extracellular matrix proteins within the renal interstitium and tubules, leading to loss of functional nephrons.
Sodium–glucose cotransporter 2 (SGLT2) inhibitor: Class of agents that reduce glucose reabsorption in the proximal tubule and exhibit renoprotective effects by modulating metabolic and inflammatory pathways.
Aquaporin-2 (AQP2): Vasopressin-regulated water channel in collecting duct cells essential for urine concentration and water homeostasis.
TGF-β1/MAPK signalling: Profibrotic cascade involving transforming growth factor-β1 and mitogen-activated protein kinases that drives myofibroblast activation and matrix synthesis.
References
- A Simplified Model of Adenine-Induced Chronic Kidney Disease Using SKH1 Mice. Cells (2024).
- Recovery of Water Homeostasis in Adenine-Induced Kidney Disease Is Mediated by Increased AQP2 Membrane Targeting. International Journal of Molecular Sciences (2024).
- Dapagliflozin alleviates renal fibrosis in a mouse model of adenine-induced renal injury by inhibiting TGF-β1/MAPK mediated mitochondrial damage. Frontiers in Pharmacology (2023).
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